• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文会议>International Symposium on PPARs : From Basic Science to Clinical Applications >Actinobacillus actinomycetemcomitans Cytolethan Distending Toxin Induces p53-independent Expression of p21 ~CIP/WAF1 and G2/M Cell Cycle Arrest in Plasmacytic Cells
【24h】

Actinobacillus actinomycetemcomitans Cytolethan Distending Toxin Induces p53-independent Expression of p21 ~CIP/WAF1 and G2/M Cell Cycle Arrest in Plasmacytic Cells

机译：Actinobacillus actinomycetemcolans cytolethan扩张毒素诱导p21〜CIP / WAF1和G2 / M细胞循环抑制的P53无关表达

获取原文
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Cytolethal distending toxin CDT which was first discovered in certain Escherichia coli strains, causes sensitive eukaryotic cells to become blocked in G2/M phase. The CDT from Actinobacillus actinomycetemcomitans also induces cell cycle arrest in G2/M phase. In the present study, the mechanism of CDT-induced cell cycle arrest was investigated using HS-72 cells, murine B cell hybridoma cell line. We found that the CDT from A.actinomycetemcomitans induced G2 cell cycle arrest in HS-72 cells by flow cytometric analysis, and that the CDT up-regulated the expression of cyclin-dependent kinase inhibitor p2I~CIP/WAF1 and tumor-suppressor protein p53. HS-72 cells transfected with the E6/E7 gene of human papilloma virus type-16, lacking the CDT induced accumulation of p53, exhibited expression of -21 ~CIP/WAF1 and G2 cell cycle arrest upon exposure to the CDT. Furthermore, octopic expression of a dominant negative p53 mutant did not inhibit the CDT mediated p21~CIP/WAF1 expression and G2 cell cycle arrest in HS-72 cells. These results indicate that the CDT-induced -53 accumulation may not be required for G2 arrest and increased level of p21~CIP/WAF1 may be important for sustained G2 cell cycle arrest and the CDT from A.actinomycetemcomitans could mediate the development of periodontal diseases through cell cycle arrest in B. lymphocytes of periodontal tissue.
机译：在某些大肠杆菌菌株中首次发现的细胞素伸展毒素CDT，导致敏感的真核细胞在G2 / m相中被封闭。来自actinobacillus的CDT诱导术中的CCOMITANS还诱导G2 / M相中的细胞周期停滞。在本研究中，使用HS-72细胞，鼠B细胞杂交瘤细胞系研究了CDT诱导的细胞周期停滞的机制。我们发现来自A.Actinomycetemco1的CDT通过流式细胞术分析诱导HS-72细胞中的G2细胞周期停滞，并且CDT上调细胞周期蛋白依赖性激酶抑制剂P2I〜CIP / WAF1和肿瘤抑制蛋白P53的表达。 HS-72细胞与人乳头瘤病毒型-16的E6 / E7基因转染，缺乏CDT诱导P53的积累，在暴露于CDT时表现出-21〜CIP / WAF1和G2细胞循环骤停的表达。此外，优势负p53突变体的章程表达不抑制CDT介导的P21〜CIP / WAF1表达和G2细胞周期停滞在HS-72细胞中。这些结果表明，G2逮捕和P21〜CIP / WAF1的增加可能不需要CDT诱导的-53积累可能对持续的G2细胞周期停滞和来自A.Actinomycetemco1的CDT可以调解牙周病的发展通过牙周组织B.淋巴细胞的细胞周期停滞。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号